International Journal of Scientific Research and Review ISSN NO: 2279-543X

A REVIEW on DIFFERENT IN-VIVO MODELS for

EVALUATION of POTENTIAL
ANTIGASTRODUODENAL ULCER AGENTS by
PRE-CLINICAL STUDIES
Nandhini B1, Shagufta Juveria2, Jeevana Jyothi S 3, Udaya Bhanu D4, Sharma J.V.C 5, V.S.S.S Gupta A6,
Deepika N7, Zoya Sameen8
1-4, 8
Joginpally B.R Pharmacy College, Hyderabad, Telangana, India.
5
Dept. of Pharmacognosy, Joginpally B.R Pharmacy College, Hyderabad, India.
6, 7
Dept. of Pharmacology, Joginpally B.R Pharmacy College, Hyderabad, India.

Abstract- Peptic ulcer is among the most serious gastrointestinal diseases in the world. Several orthodox drugs are employed for the
treatment of the disease. Although these drugs are effective, they produce many adverse effects thus limiting their use. In recent
years, there has been a growing interest in alternative therapies, especially those from plants due to their perceived relative lower side
effects, ease of accessibility, and affordability. Advanced in the discovery of more effective and safe anti-ulcer agent is due to the
introduction of large number of newer experiment methods to evaluate their anti-ulcer activity in different types of gastric ulcers.
Advanced in the discovery of more effective and safe anti-ulcer agent is due to the introduction of large number of newer experiment
methods to evaluate their anti-ulcer activity in different types of gastric ulcers. In this paper, current in vivo animal models of ulcer as
well as the challenges associated with their use have been discussed.

Keywords- Gastric Ulcer; Ulcer Score; Ulcer Index; Percentage Protection; Percentage Inhibition; Non-Steroidal Anti-Inflammatory
Drugs

I. INTRODUCTION
Peptic ulcer diseases comprise heterogeneous disorders, which manifest as a break in the lining of the gastrointestinal mucosa bathed by acid
and pepsin. It is the most predominant of the gastrointestinal diseases with a worldwide prevalence of about 40% in the developed countries
and 80% in the developing countries. It is generally recognized that peptic ulcer is caused by a lack of equilibrium between the gastric
aggressive factors and the mucosal defensive factors [1]. Based on site of attack, it can be classified mainly into four types they are gastric,
duodenal, esophageal and Meckel's Diverticulum ulcers. Gastric ulcer is a peptic ulcer that develops in the stomach. Duodenal and esophageal
ulcers occur in the duodenum and esophagus respectively. Meckel's Diverticulum ulcer is a less common type of ulcer that develops in the
Meckel's Diverticulum (a vestigial remnant in the form of a small bulge in the small intestine) [2]. The etiology of gastroduodenal ulcers is
influenced by various aggressive and defensive factors such as acid-pepsin secretion, parietal cell, mucosal barrier, mucus secretion, blood
flow, cellular regeneration and endogenous protective agents (prostaglandins and epidermal growth factors). According to Peckenpaugh and
Poleman, some other factors, such as bad dietary habits, excessive intake of Non-steroidal anti-inflammatory agents, stress, hereditary
predisposition and Helicobacter pylori infection, which is reported to account for more than 70% of cases, are responsible for the development
of peptic ulcer diseases.
Currently, a comprehensive paper is available for an in vitro model for Helicobacter pylori, and can be employed to evaluate
medicinal plants for anti-peptic ulcer activity. The current paper, focuses on discussions of models for in vivo peptic ulcers, the mechanisms
underlying their induction and indices used to measure the extent of the induced ulcers [1].

II. EXPERIMENTAL PEPTIC ULCER MODELS

Peptic ulcers can be induced by physiological, pharmacological or surgical manipulations in several animal species. However, most
experiments in peptic ulcer studies are carried out in rodents. Several models are used experimentally for testing or evaluating antipeptic ulcer
activity of drugs/agents, and these include the following:

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A. Water-immersion stress or cold-water-restraint or cold-restraint stress

B. NSAIDs-(indomethacin, aspirin, and ibuprofen) induced gastric ulcers
C. Ethanol-induced gastric ulcers
D. Acetic acid-induced gastric ulcers
E. Pylorus-ligated-induced peptic ulcers
F. Cysteamine-induced duodenal ulcers
G. Indomethacin-histamine induced duodenal ulcers
H. Histamine induced gastric ulcers
I. Reserpine induced ulcers
J. Serotonin-induced gastric ulcers
K. Diethyldithiocarbamate-(DDC)-induced peptic ulcers
L. Methylene blue-induced ulcers
M. Ischemia-reperfusion-(I-R-) induced gastric ulcers
N. Ferrous iron-ascorbic acid-induced gastric ulcers
O. Acetic acid-H. Pylori-induced ulcers

A. WATER-IMMERSION STRESS OR COLD-WATER-RESTRAINT OR COLD-RESTRAINT STRESS [3]

Gastric ulcers induced by water–immersion stress or cold resistant stress in rats or mice are known to resemble human peptic ulcers, both
grossly and histopathologically. The restraint technique developed by Brodie and Hanson when coupled with the cold water or ordinary water
immersion method developed by Levine is reported to induce stress lesions in a synergistic manner. Stress induced ulcers are mediated mainly
by the release of histamine that results in an increased acid secretion, decreased mucus production, pancreatic juice reflux and poor flow of
gastric blood. Generation of reactive oxygen species and inhibition of prostaglandin synthesis also promote stress induced ulcer formation.
This model has been widely used for assessing the gastro protective effects of various test agents especially those with mucus enhancing
properties. In water-immersion stress model, animals are fasted for a period of 24-36 h prior to the experiment and treated with vehicle or test
drug or reference drug. After 30 min. animals are placed individually in each compartment of a stress cage and immersed vertically up to the
xyphoid level in a water bath and kept for 7 hrs to induce stress ulcer. After 7 hrs animals are sacrificed and ulceration quantified. In cold
resistant stress model animals are fasted for a period of 18 hrs prior to the experiment treated with vehicle. After 1 hr, rats are individually
restrained in plastic cages in a refrigerator for 2-4 hrs and sacrificed. Finally, stomachs are taken out and severity of ulceration is measured.
B. NSAIDS-(INDOMETHACIN, ASPIRIN, AND IBUPROFEN) INDUCED GASTRIC ULCERS [4]
We used an NSAIDs -induced gastric ulcer model. NSAIDs was administered orally in graded doses (10 mg/kg, 25 mg/kg, 50 mg/kg,
100 mg/kg, and 200 mg/kg) to detect the best effective antiulcer dose of NSAIDs. The parameters measured were: ulcer index,
histopathological scoring of gastric ulcer, gastric juice analysis, gastric mucosal lipid peroxidation parameters, estimation of NO metabolite in
blood, mRNA expression of inducible nitric oxide synthase (iNOS) and constitutive NO synthase (cNOS) in gastric mucosa, and gastric
mucosal DNA fragmentation.
C. ETHANOL-INDUCED GASTRIC ULCERS [5]
After 24 hrs fasting, the rats were divided into seven groups of six animals each. The group I served as a normal control, given 1% CMC in
water (5 ml/kg, p.o), Group II was treated orally with omeprazole (30 mg/kg), Group III and V orally received 250 mg/kg of petroleum ether
and methanol extract respectively, while Group IV and VI orally received 500 mg/kg of petroleum ether and methanol extract respectively.
Group VII received 100 mg/kg of TSF. After 45 min, ulceration was induced by oral administration of 1 ml of absolute ethanol. Animals were
sacrificed after 1h following the administration of absolute ethanol.
D. ACETIC ACID-INDUCED GASTRIC ULCERS [6]
Male Sprague-Dawley rats weighing approximately 200 g were used for this study. They were assimilate in the animal house for one week
prior to the study. Chronic gastric ulcers were produced by direct application of acetic acid using a modification of the method previously
described by Okabe and Konturek. General Anesthesia was induced by intraperitoneal administration of pentobarbitone 35 mg/kg.
Laparotomy was performed through a midline epigastric incision and the stomach exposed. A plastic mould of 10 mm diameter was applied
tightly to the serosal surface of the anterior wall of the stomach just proximal to the antrum and glacial acetic acid was poured through the
mould onto the surface of the stomach for 20 seconds. The procedure was then repeated for the posterior wall of the stomach. The abdomen

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was closed with catgut and silk. The body temperature of the animals was kept at 37°C and the animals were allowed to recover from the
anesthesia. They were then divided into four groups and given unlimited normal diet and water for the next seven days. The animals were
divided into four groups and treated daily by gavage with either 1 ml of solvent, 5 mg of capsaicin in 1 ml of solvent, 40 mg of cimetidine in 1
ml of solvent, or 5 mg of capsaicin plus 40 mg of cimetidine in 1 ml of solvent. At the end of one week, the animals were killed and their
stomachs removed, opened along the greater curvature, fixed in 10% neutral buffered formalin overnight, and photographs taken. The area of
the entire gastric mucosa and any ulcers that were present were measured with a digital planimeter by an observer who was unaware of which
group each animal belonged to under the curve were derived in arbitrary units for quantification of gastric mucosal blood flow over defined
time periods.
E. PYLORUS-LIGATED-INDUCED PEPTIC ULCERS [7]
In 36 hrs fasted rats pylorus ligation were performed under light ether anesthesia, care being administered orally immediately after pylorus
ligation. After 19 hrs. ligation, the rats were sacrificed. The stomachs were removed and opened along the greater curvature. The glandular
portion of stomach was observed for measurement of ulcer index. The contents were drained into tubes, centrifuged and subjected to analysis
for various biochemical parameters. The volume and pH of gastric juice were measured. Total acidity, Total acid output, Pepsin activity, total
carbohydrate and protein content were estimated. Finally, the total carbohydrate to protein (TC/PR) ratio i.e., mucin activity was derived.
Gastric wall mucus content (GWMC) was measured from glandular portion of stomach and was expressed as mg of alcian blue per g of wet
glandular tissue.
F. CYSTEAMINE-INDUCED DUODENAL ULCERS [8]
In Cysteamine-induced duodenal ulcer model, PCE and cimetidine showed significant reduction in the total lesion area when compared with
control group. 50% ethanolic extract of patol churna showed significant antiulcer effect against ethanol and aspirin-induced gastric ulcers.
Ethanol administration may evoke gastric secretion through a more direct action on the stomach, involving the release of gastrin, histamine
and endogenous endothelin (ET-1) from vascular endothelial cells in the fundic mucosa. Also, certain prostaglandins are capable of protecting
rats against gastric mucosal lesions caused by necrotizing agents like ethanol and strong acid. Aspirin has been recorded to cause mucosal
damage by several factors such as inhibiting prostaglandin synthesis, enhancing acid secretion, increasing back diffusion of H+ ions,
decreasing mucin secretion and breaking of mucosal barrier. Thus, the antiulcer activity of the patol churna extract in these models can be
related to the cytoprotective action. Gastric hypersecretion plays an important role in production of experimental ulcers by pylorus ligation
increased biosynthesis of nucleic acids and increased metabolism of carbohydrates and thereby exhaustion of carbohydrates and other
compensatory mechanisms could also be responsible for ulceration due to pylorus ligation. It is evident from the biochemical parameters that
PCE has antiulcer effect in pylorus ligation model. The mechanism of their antiulcer activity can be related to the acid neutralizing property,
reduction in acid-pepsin secretion and increase in mucin activity. Cysteamine-induced ulcers are considered to be due to continuous
hypersecretion of gastric acid. The pathogenesis of cysteamine induced duodenal ulcers includes enhanced gastric acid secretion, increased
duodenal motility delayed gastric emptying and decreased duodenal bicarbonate secretion in response to acid. It is suggested from our results
that patol churna and cimetidine possess significant anti-duodenal ulcer activity. The mechanism of this activity can be related to inhibitory
effect of acid and pepsin activity.
G. INDOMETHACIN-HISTAMINE-INDUCED DUODENAL ULCERS [9]
We standardized a new method for producing duodenal ulcers in rats by administering indomethacin plus histamine, and investigated the
pathogenesis. Indomethacin (5 mg/kg) was first given subcutaneously to rats fasted for 24 h, and subsequently histamine dihydrochloride (40
mg/kg) was given subcutaneously three times, at 2.5-h intervals, beginning 30 min after injection of indomethacin. This combined treatment
induced one or two round lesions (9.8 ± 1.4 mm2) in the proximal duodenum at an incidence of 100%, and a few lesions in the corpus and
antrum of the stomach as well. Indomethacin or histamine alone had no effect on either the duodenum or the stomach. The lesions in the
duodenum and antrum were inhibited by oral cimetidine (3-100 mg/kg) and 16,16-dimethyl prostaglandin E2 (dmPGE2 ) (3-30 g/kg) in a
dose-related manner, whereas those in the corpus were inhibited only by cimetidine. Indomethacin alone had no effect on gastric acid
secretion, but did potentiate the increase of acid secretion caused by histamine. Histamine did not affect duodenal HC03- secretion, whereas
indomethacin slightly inhibited the basal HC03- secretion and completely blocked the acid stimulated HC03- secretion. Intraduodenally
administered cimetidine (30 mg/kg) or dmPGE2 (30 j-30µ/kg) significantly inhibited acid secretion or increased HC03- secretion,
respectively, and both reduced the amount of acid emptied into the duodenum after treatment with indomethacin plus histamine. These results
indicate that the development of duodenal lesions induced by indomethacin plus histamine in rats is due to both an increase in gastric acid

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secretion and an impairment of acid-induced duodenal HC03- secretion. This newly established model will be useful for studying the
pathogenesis of duodenal ulcers and for screening antiulcer agents.
H. HISTAMINE-INDUCED GASTRIC ULCERS [10]
Histamine released from mast cells and binds with receptors present on the surface of parietal cells which leads to activation of adenyl
cyclase. This adenyl cyclase converts ATP into c-AMP. This conversion enhances secretion of HCL from parietal cells .
Male Guinea pigs are used for the experiment. Animals are fasted for 36 hours. Histamine acid sulphate in dose of 50mg is injected
intraperitonially.
 To prevent histamine toxicity, promethazine hydrochloride in dose of 5mg is injected intraperitonially 15 minutes before and 15
minutes after the histamine injection.
 Test drug is administered 30-45 minutes later of histamine injection.
 After 4 hours, animals are sacrificed, stomach removed and dissected.
 Ulcer index is calculated to examine the severity of ulcers.
I. RESERPINE-INDUCED GASTRIC ULCERS [10]
1. PRINCIPLE: Reserpine acts on cholinergic system. Reserpine increases histamine secretion by causing degranulation of gastric
mast cells
2. PROCEDURE: Female Sprogue- Dawley rats are used for the experiment.
 Animals are fasted for 48 hours.
 Test drug is administered intraperitonially.
 Half an hour later, reserpine in dose of 15 mg/kg is administered intraperitonially.
 4 hours later, animals are sacrificed, stomach are removed and dissected.
 Ulcer index is calculated.
J. SEROTONIN-INDUCED GASTRIC ULCERS [10]
1. PRINCIPLE: Serotonin acts as vasoconstrictor which reduces gastric mucosal blood flow and leads to acute mucosal injury.
2. PROCEDURE: The wistar albino rats were randomly assigned in to 5 groups of 6 animals each. Serotonin creatinine sulphate
(20mg/kg) is administered subcutaneously to rats (24hr fasted). Alcoholic extract and petroleum ether extract of mimusops elengi or
controlled vehicle is administered orally 30 min prior to serotonin injection. The animals were sacrificed after 18hr, their stomachs were
removed and the ulcer index is determined.

K. DIETHYLDITHIOCARBAMATE-(DDC)-INDUCED PEPTIC ULCERS [10]

1. PRINCIPLE: DDC induces ulcers through the mobilization of super-oxide and hydroxyl radicals. Super-oxide radicals and
hydroxyl radicals plays a pathogenic role in development of ulcers.
2. PROCEDURE: This model is used to assess the anti-oxidative activity and cyto-protective activity of drug.
 Animals are fasted for 24 hours.
 Acute glandular lesions are induced by subcutaneous injection of 1ml of DDC in saline followed by oral dose of 1ml of
0.1N HCl.
L. METHYLENE BLUE-INDUCED ULCERS [10]
1. PRINCIPLE: Methylene blue is a synthetic drug. It is known to generate super-oxide radical ions by uncoupling of ATPase. In
addition it also have anti-cholinergic activity. Drugs with anticholinergic activity and proton pump inhibitory activity can be assessed by using
this model.
2. PROCEDURE:
 Animals are fasted for 24 hours.
 Methylene blue is administered at a dose of 125mg/kg of body weight orally followed by the administration of test drug.
 Animals are sacrificed after 4 hours of methylene blue administration.
 Stomachs are dissected out and ulcer index is calculated.

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M. ISCHEMIA-REPERFUSION-(I-R-) INDUCED GASTRIC ULCERS [10]

1. PRINCIPLE: Reperfusion of gastro intestine following ischemia leads to formation of free radicals which results in
development of erosion and ulceration in the gastric mucosa.
2. PROCEDURE:
 Animals are fasted for 24 hours.
 Animals are anesthetized.
 Laparotomy is performed and esophageal and pyloric ends of the stomach are clamped using bull god clips.
 Celiac artery is then clamped at a point of 0.5 cm distal from the branch to the aorta for 30 min.
 Reperfusion in GI is for 20 min.
 Animals are sacrificed, stomachs are dissected out and ulcer index is calculated.
N. FERROUS IRON-ASCORBIC ACID-INDUCED GASTRIC ULCER [1]
1. MODEL: This type of gastric ulcer model is induced by the local injection of ferrous iron with ascorbic acid (Fe/ASA) solution
into the gastric wall. The ulcers produced resemble human gastric ulcers that penetrate the muscularis mucosa. Lipid peroxidation mediated by
oxygen radicals plays a crucial role in the pathogenesis of the gastric ulceration induced by the Fe/AS.
O. ACETIC ACID-H. PYLORI-INDUCED ULCERS [1]
Rats can also be ulcerated with acetic acid according to the method described by Takagi et al. Under anesthesia, laparotomy is performed in
rats through a midline epigastric incision, the stomach is exposed, and 20% of acetic acid (0.03 mL) is injected into the sub serosal layer of the
glandular portion, using a micro syringe (0.05 mL). After closing the abdominal incision, the animals are maintained in individual cages, with
daily access to commercial food restricted to the time periods of 9-10 a.m. and 5-6 p.m. This allows for adequate fasting for administration of
Helicobacter pylori, drugs or agents under investigation as well as standard drugs (amoxicillin (AMX) 50 mg/kg + clarithromycin (CLR) 25
mg/kg with a proton pump inhibitor such as omeprazole 20 mg/kg). According to Konturek et al., 24 hours after ulcer induction by acetic
acid, animals are inoculated intragastrically with 1 mL of confirmed pathogenic strain of Helicobacter pylori such as ATCC 43504 (9 × 108)
suspended in Mueller Hinton broth or Brain-Heart Infusion Broth by using a cannula appropriate for orogastric gavage. For the animals in the
control, and Acetic Acid-induced ulcer groups without Helicobacter pylori infection, only Mueller-Hinton or Brain Heart Infusion Broth is
administered orally. The orogastric inoculation with Helicobacter pylori is done twice a day for 7 days, whereas the test drugs/agents, control
and standard drugs, are administered twice a day, for 14 consecutive days, starting from the third day after ulcer induction by acetic acid.
After treatment, the animals are sacrificed by cervical dislocation, blood is collected from the inferior vena cava, and the stomachs are
removed for evaluation of gastric lesions.
III. MEASUREMENT OF GASTRIC LESIONS
The ulcer index, the percentage protective ratio, and the percentage curative ratio are, respectively, given by the following equation:

Ulcer index (UI) =

.
( ) ( )
Percentage protective ratio = −
( ) ( )
( ) ( )
Percentage curative ratio = ( )
− ( )

Another method is where the total ulcerative area in relation to the total area of each stomach is used in determining the ulcer index as
described by Ganguly:

Relative Area =

Using the method described by Dekanski et al., the severity of the mucosal lesions can also be assessed and the ulcer index is scored as
follows:
  0 = no damage,
  1 = blood at the lumen,
  2 = pinpoint erosions,

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  3 = one to five small erosions <2 mm,

4 = more than five small erosions <2 mm, 
5 = one to three large erosions >2 mm,
6 = more than three large erosions >2 mm.
The ulcer index, the percentage protection ratio, and the percentage curative ratio are, respectively, given by the following equation:

Ulcer index [UI] =

.

Percentage protective ratio = −

Percentage curative ratio = −

Another method used is described by Desai et al. In this method which is based on the intensity of lesions, ulcers are given scores as follows: 
0 = no ulcer, 
1 = superficial mucosal erosion,
2 = deep ulcer or transmural necrosis,
3 = perforated or penetrated ulcer.
The ulcer index, the percentage protective ratio, and the percentage curative ratio are, respectively, given by the following equations:

Ulcer index [UI] = + X2

.

Percentage protective = X100

Percentage curative = X100

According to the method by Nwafor et al. The observation of erosions and scores made as 1–5 as follows;
1 = small round hemorrhagic erosion,
2 = hemorrhagic erosion <1 mm,
3 = hemorrhagic erosion of 2-3 mm,
5 = hemorrhagic erosion >4 mm.
The scores are multiplied by 2 when the width of the erosion is larger than 1 mm
The ulcer index, the percentage protective or inhibition ratio, and the percentage curative ratio are, respectively, given by the following
equations:

Ulcer index [UI] =

.

Percentage protective or inhibition = −

Percentage curative = −

According to the method by Kulkarni, the ulcer index can be measured or registered using the following scores involving the number and
severity of ulcers:
0.0 = normal colored stomach,
0.5 = red coloration,
1.0 = spot ulcers,
1.5 = hemorrhagic streaks,
2.0 = ulcers with area >3 but ≤5 mm2, 
3.0 = ulcers > 5 mm2,
Ulcer index [UI] = UN +US+UP×10
Where UI = ulcer index, UN = average number of ulcers per animal, US = average of severity score, and UP = percentage of animals with
ulcer.
The percentage protective ratio, and the percentage curative ratio are, respectively, given by the following equation:
[ ]
Percentage protective ratio = 100 − X100
[ ]
[ ]
Percentage curative ratio = 100 − 𝑥100
[ ]

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According to the method by Andrade et al., ulcers are classified as;

level I ulcer area < 1 mm2,
level II ulcer area = 1–3 mm2,
level III ulcer area > 3 mm2
The following parameters are determined:
Ulcerative lesion index [ULI] = 1X (number of ulcers level I) + 2X(𝑛𝑢𝑚𝑏𝑒𝑟 𝑜𝑓 𝑢𝑙𝑐𝑒𝑟𝑠 𝑙𝑒𝑣𝑒𝑙 𝐼𝐼) + 3X(𝑛𝑢𝑚𝑏𝑒𝑟 𝑜𝑓 𝑢𝑙𝑐𝑒𝑟𝑠 𝑙𝑒𝑣𝑒𝑙 𝐼𝐼𝐼 )
[
Percentage protective ratio = 100 − 𝑋100
[ ]
[ ]
Percentage curative ratio = 100 − 𝑋100
[ ]

In all of these ways of determining ulcer indices, attempts are made to find a solution to the problem of incomplete quantification of gastric
and duodenal ulcers. Different scoring systems have been described for use to measure gastro-duodenal ulcerations and calculate ulcer
indices. In the method described by Takagi and Okabe, the number of ulcers rather than the size of ulcers is given importance for assessing
ulcer severity. Implicitly, the approach may yield results that may be statistically correct in terms of the number of ulcers but will be
biologically irrelevant. Several researchers, through their studies, have tried to reduce the level of biological incorrectness in ulcer
quantification. For example, the method by Nwafor et al. measures only the length of the erosive ulcers without considering the total area of
ulcerations in relation to the total mucosal area. Others have tried to distinguish the different types of lesions or ulcerations such as spot ulcers,
haemorrhagic streaks, deep ulcers, and perforated ulcers. However, the areas of ulcerations fail to have consideration in most of the
parameters used. Andrade et al. in an attempt to improve on the biological correctness of ulcer indices factored into their assessment the areas
of ulceration and categorized them into levels I, II and III based on size of the ulcers. Despite the improvement on the methods described by
others the approach suffers a pitfall as it does not consider the total area of the stomach in determining the ulcer index. The procedure would
therefore, produce a statistically correct ulcer index that would not be biologically relevant. It would seem then that, the method described by
Ganguly although quiet old, would be better than others in the literature as it takes into consideration the total area of the stomach in relation
to the total area of the ulceration in determining the ulcer index. Although this procedure also overlooks the level of erosion
histopathologically in the quantification of ulcers, in our opinion, the method described by Ganguly produces ulcer indices that are close to
being both biologically and statistically relevant.
IV. CONCLUSIONS
Ulcer is an important gastrointestinal disease that mainly caused by H. Pylori infection and high intake of NSAIDs. Pre-clinical evaluation of
new or existing anti-ulcer drug can be done by using appropriate In-Vivo models. We have also discussed currently avail-able methods for
scoring ulcers, pointing out the pitfalls in the various approaches. Several experimental ulcer models, which can be used for testing potential
antiulcer agents such as plant medicines that are reported to have ethnomedicinal uses against ulcers.
ACKNOWLEDGEMENT
The authors are thankful to management, principal and vice-principal of Joginpally B.R Pharmacy College, Hyderabad, for kind support
throughout our study.
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Nyarko, Hindawi Publishing Corporation, Ulcers vol. 2013, Article 796-405, 12 pages
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Scholars Research Library, 2011, 3(2): 180-186
[3] “An Overview of In Vitro and In Vivo Models that can be used for Evaluating Anti-Gastric Ulcer Potential of Medicinal Plants, “Thabrew MI1 and
Arawwawala LDAM2, Austin Biology, Austin Biol- 2016 Volume 1(2).
[4] “Gastroprotective effect of benzafibrate, a peroxisome proliferator activated receptor α agonist and its mechanism in a rat model of aspirin-induced gastric
ulcer”, LekhaSaha, AlkaBhatia, Amitava Chakrabarti”
[5] “Antiulcerogenic effects of spathodea falcata against different experimental models” A.S. Jain, S.J. Surana, Asian Journal of Pharmaceutical and Clinical
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Homoeopathy and Ayurvedic Medicine, 2011, Volume 1, Issue 1, 1000105

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[7] “Á Effect of capsaicin and cimetidine on the healing of acetic acid induced gastric ulceration in the rat”, J Y Kang, C HTeng, F C Chen, PMC
[8] “A new model of duodenal ulcers induced in rats by indomethacin plus histamine,” Koji Takeuchi, Osamu Furukawa, Hironori Tanaka, Susumu Okabe, The
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[9] “In-Vivo Models Used for Pre-Clinical Evaluation of Anti-Ulcer Activity,” Meena DK and Jayanthi M, Austin Pharmacology and Pharmaceutics, 2018,
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